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Non-Invasive Transcutaneous
Pacing
Application Note
Introduction
This Application Note provides an overview of
non-invasive transcutaneous pacing. It includes a brief
history of pacing, describes the electrical activity of the
heart, and explains how pacing works.
Non-Invasive Transcutaneous Pacing
What is Non-Invasive Transcutaneous Pacing?
Non-invasive transcutaneous pacing is a technique of
electrically stimulating the heart externally through a set
of electrode pads. The stimulus is intended to cause
cardiac depolarization and myocardial contraction.
Pacing is one method of treating patients when their
heart’s own conduction system slows dangerously.
Electrical Activity of the Heart
The unique physiologic characteristics of cardiac muscle
cells produce intrinsic pacing and efficient conduction,
leading to optimal synchrony and contractility (see
Figure 1).
Figure 1
The Cardiac Cycle 1
These pathways consist of highly specialized myocardial
cells which have the ability to conduct a depolarization
wave at a much greater velocity than ordinary myocardial
cells.
R
T
P
The normal sequence of myocardial depolarization and
contraction, is described below:
Q
S
Atrial systole
0.0
.1
In order for the heart to beat with a smooth and efficient
pumping action, the various parts of the myocardium
must contract in a well-defined sequence. The atria must
contract before the ventricles, the ventricles must begin
contracting near the apex, etc. An orderly sequence of
contraction during systole is provided for by specialized
conductive pathways in the myocardium.
Ventricular systole
.2
.3
.4
.5
Approximate time (sec)
Diastole
.6
1.
.7
.8
Figure 2
The myocardial cell membrane, like the membranes of
other muscle cells in the body, has the ability to conduct
a propagated action potential or depolarization wave.
Likewise, depolarization of the myocardial cell
membrane by a propagated action potential results in
myocardial contraction. The propagation of an action
potential can be initiated by intrinsic automaticity, direct
electrical stimulation (i.e. transvenous or transthoracic
pacing), or by a transmitted external stimulus.
The cardiac cell membrane does not require an external
stimulus to reach threshold. It possesses a special ability
that allows it to spontaneously depolarize at periodic
intervals without the need for an external stimulus. This
property is called automaticity.
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A cluster of highly conductive cells called the
sino-atrial (SA) node is located near the back wall of
the right atrium (see Figure 2). It is at the SA node
that the depolarization wave is normally initiated.
Normal Myocardial Sequence
SA
2.
From the SA node, the depolarization wave passes
from right to left over both atria, resulting in atrial
systole. Within 70 ms, all portions of both atria have
started to contract.
Electrical Activity of the Heart
3.
The atrio-ventricular (AV) node consists of a cluster
of cells leading from the lower portion of the right
atrium to the ventricular septum (see Figure 3). The
AV node is highly specialized and conducts the
depolarization wave very slowly. It delays its progress
for approximately 70 ms, which allows atrial systole
to reach completion before ventricular systole begins.
Figure 3
AV Node
AV
Because our bodies require more oxygen during periods
of physical and emotional stress, the SA node is liberally
supplied with nerve endings which can stimulate its cells
more rapidly when necessary. Hence, during periods of
excitement, the SA node responds with a faster rate of
depolarization and the heart rate increases to ensure the
muscles have enough oxygen to cope with the sudden
demand.
The properly functioning Bundle of His and Purkinje
network ensure that the heart always contracts
rhythmically, and therefore pumps efficiently. The fact
that all conductive cells in the heart possess the capability
of spontaneous depolarization provides a natural back-up
pacemaking capability, in case the SA node should fail.
The progress of the depolarization wave causing the
muscle contraction can be followed and recorded. The
recorded ECG waveforms and their correlation to the
activity of the heart are illustrated in Figures 1 through 7.
The depolarization of the atria is represented by the
P-wave (Figure 4). During this time, the atria contract
and force blood into the ventricles. At the point labeled
“Q”, the ventricles begin depolarizing and contracting.
4.
5.
From the AV node, the depolarization wave moves to
the Bundle of His and its bundle branches. These lie
in the ventricular septum and conduct the
depolarization wave to the apex of the heart.
From the bundle branches, the depolarization wave
rapidly travels through the Purkinje network, a fine
mesh of highly conductive fibers that cover the
endocardial (inner) surfaces of both ventricles.
6.
At this point, depolarization and contraction of the
ventricular myocardium begin. From the Purkinje
network, the depolarization wave moves through the
ventricular myocardium from the endocardial (inner)
to the epicardial (outer) surfaces. Because of its course
of travel through the bundle branches and Purkinje
network, myocardial contraction begins in the
ventricular septum, then moves rapidly to the apex of
the heart and finally proceeds towards the base.
7.
As soon as the cells in the myocardium have
depolarized, they begin entering the refractory state
and repolarizing. They rest until the next stimulus,
which under normal conditions, is supplied by the
cells in the SA node.
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Figure 4
Atrial Depolarization
P-Wave
R
Q S
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Non-Invasive Transcutaneous Pacing
Notice the time delay between the P-wave and Q. This is
the 70 ms delay introduced by the AV Node (Figure 5).
The “T” wave represents the refractory period of the
heart when the ventricles are repolarizing (Figure 7).
Figure 5
Figure 7
AV Node Delay
Ventricular Repolarization
R
PR-interval
Q S
The time between “Q” and “S” (called the QRS
complex) immediately precedes full contraction of the
ventricles when blood is forced into the arterial system
(Figure 6).
Figure 6
Ventricular Depolarization
QRS-complex
Application of Pacing
Disease in the conduction system or failure in the
automaticity of the myocardial cells can lead to
symptomatic bradycardia or other arrhythmias which
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may necessitate pacing intervention.
T-wave
Application of Pacing
The following table explains the indications and
symptoms of emergency pacing.
Table 1
Indications of Emergency Pacing and
Pacing Readiness 6
Immediate Emergent Pacing
Class I
Hemodynamically symptomatic, compromising
bradycardias that are too slow and unresponsive to
atropine.a Symptoms can include blood pressure less
than 80 mmHg systolic, change in mental status,
angina, pulmonary edema.
Class IIa
Bradycardia with escape rhythms unresponsive to
pharmacologic therapy
Pacing for patients in cardiac arrest with profound
bradycardia or PEAb due to drug overdose, acidosis,
or electrolyte abnormalities
Standby pacing: prepare for pacing for specific
AMI-associatedb rhythms:
•
•
•
•
Symptomatic sinus node dysfunction
Mobitz type II second-degree heart block
Third degree heart block c
Newly acquired left, right, or alternating BBBb or
bifascicular block
Class IIb
Override pacing of either supraventricular or
ventricular tachycardia that is refractory to
pharmacologic therapy or electrical cardioversion
Bradyasystolic cardiac arrest
a. Including complete heart block, symptomatic second-degree
heart block, symptomatic sick sinus syndrome, drug-induced
bradycardias (i.e., amiodarone, digoxin, β-blockers, calcium
channel blockers, procainamide), permanent pacemaker
failure, idioventricular bradycardias, symptomatic atrial
fibrillation with slow ventricular response, refractory
bradycardia during resuscitation of hypovolemic shock, and
bradyarrhythmias with malignant ventricular escape
mechanisms.
b. PEA indicates pulseless electrical activity;
AMI, acute myocardail infarction; and
BBB, bundle branch block.
c. Relatively asymptomatic second- or third-degree heart block
can occur in patients with an inferior myocardial infarction. In
such patients pacing should be based on symptoms of
deteriorating bradycardia.
Fixed Rate or Demand
Pacing—Which One To Use?
Many non-invasive transcutaneous pacemakers operate
in two modes: fixed rate (also referred to as asynchronous
or non-demand) and demand mode (also referred to as
synchronous).
Fixed Rate Mode Pacing
In the fixed rate mode, the pace rate is set by the clinician
regardless of the patient’s intrinsic heart rate. This option
is preferable when the ECG signal becomes extremely
noisy due to motion artifact or when the pacemaker is
sometimes unable to sense the intrinsic beat.
Another reason for using the fixed rate mode is to
terminate tachyarrhythmias by overdriving the patient’s
intrinsic beat. This method has been successful in a
limited number of patients7,8,9. The above methods are
not widely used in a clinical setting. The danger with
fixed rate mode pacing is the possibility of further
exacerbating the tachyarrhythmia and triggering
ventricular fibrillation9. Fixed rate mode does not sense
the QRS complex for the R-wave and may pace on the
T-wave, which could trigger ventricular fibrillation.
Demand Mode Pacing
In demand mode pacing, the pacer senses the patient’s
intrinsic heart rate and will pace if the intrinsic signal is
slower than the rate programmed by the clinician.
For example, if the patient’s heart rate becomes slower
than the prescribed setting, the pacer will send an
electrical stimulus. If the pacer senses that the heart rate
is faster than the pacing rate, it inhibits an electrical
signal. The advantages of demand mode pacing are:
competition between the pacemaker stimuli and the
intrinsic heart rate is minimized, decreasing the risk of R
on T, and the number of pace pulses introduced are
minimized reducing patient discomfort. For this reason,
demand mode pacing is primarily used as the default
setting.
During demand mode pacing, Philips’ HeartStart ALS
defibrillators detect R waves, or beats. Intrinsic beats are
defined as those that are generated naturally by the
patient. Paced (or captured) beats are defined as those
that are a result of delivered pacing energy.
Philips’ ALS defibrillators also define the paced refractory
period, which is simply a period of time after the delivery
of a pace pulse. The refractory period is approximately
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Non-Invasive Transcutaneous Pacing
340 ms for pacing rates less than or equal to 80 pulses per
minute (PPM), and approximately 240 ms for pacing
rates greater than or equal to 90 PPM.
With the pacer on, the defibrillator marks intrinsic beats
on the R-wave with a marker on the MRx and an arrow
the XL+. The intrinsic beats are also marked in the print
strip. When an intrinsic beat is detected, the time interval
for the next pace pulse starts at the intrinsic beat. If no
intrinsic beat is detected, the time interval for the next
pace pulse starts at the last pace pulse.
Philips HeartStart MRx and HeartStart XL+
defibrillators use the ST/AR Basic Arrhythmia Algorithm
for arrhythmia analysis. This analysis provides
information on your patient's condition, including heart
rate and arrhythmia alarms. The lead appearing in Wave
Sector 1 is used for arrhythmia analysis. Because the
ST/AR Basic Arrhythmia Algorithm is the source needed
to generate heart rate and heart rate alarms, the algorithm
cannot be disabled. However, if desired, arrhythmia and
heart rate alarms can be turned off. During arrhythmia
analysis, the ECG monitoring parameter continuously:
•
Optimize ECG signal quality to facilitate arrhythmia
analysis. The ECG signal is continuously filtered to
remove baseline wander, muscle artifact, and signal
irregularities.
•
Measure signal features such as R-wave height, width,
and timing.
•
Create beat templates and classify beats to aid in
rhythm analysis and alarm detection.
•
Examine the ECG signal for ventricular arrhythmias
and asystole.
It is impossible to design a computerized arrhythmia
algorithm that accurately identifies R-waves 100% of the
time. Several conditions can cause difficulty for the
algorithm to interpret R-waves, such as tall P-waves, tall
T-waves, aberrantly conducted beats, and P-waves
without a conducted R-wave that follows. In most
instances, tall T-waves and P-waves can be addressed by
selecting different leads to minimize the P-wave or
T-wave amplitudes relative to the R-wave amplitude.
You may choose to display an annotated ECG with
ST/AR arrhythmia beat labels in Wave Sector 2. The
same ECG source appearing in Wave Sector 1 may be
displayed with a six-second delay along with white
arrhythmia beat labels. The R-waves marked in Wave
Sector 1 are annotating the intrinsic beats that control
the demand pacing function. The R-waves marked with
beat labels in Wave Sector 2 control the analysis and
arrhythmia alarms.
Clinicians must not rely solely on the defibrillator’s
classification of beats as intrinsic or paced to determine
electrical capture. Consider the situation where the
patient's intrinsic HR is 62, and the pacer is set at a rate
of 60. Since the two rates are very close, pacer spikes and
intrinsic beats may occur very close to each other for
several seconds. In this circumstance, the defibrillator
may think the beats are paced based on its simple timing
algorithm, but in fact the beats are intrinsic and the
timing coincidental. There may also be cardiac
conditions which can cause a truly paced beat to fall
outside of the refractory period.
Capture must be determined by a clinician who is trained
to interpret the ECG being displayed by the defibrillator.
The defibrillator's marking of beats can be used as a
guide, but not as an absolute indication, of whether or
not capture has been achieved.
How to Implement Non-Invasive Pacing
Pads Application and Placement
Before applying the pads, clean and dry skin sites with a
towel. It may be necessary to shave or clip excessive hair
in the area of the pads. Follow the manufacturer’s
suggested placement of electrode pads. Do not reverse
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the pads since reversing electrode pad placement
increases the pacing threshold. Thus, more current will
be needed to capture the heart resulting in greater patient
discomfort10. The most common electrode placement is
the anterior-anterior position (Figure 8).
How to Implement Non-Invasive Pacing
Figure 8
Anterior-Anterior Position
data card, and the date and time may be changed.
However, a password is required to change the
configuration of the device. When modifying
configuration settings, the device should be connected to
external power and have a battery with at least 20%
capacity installed.
Further reference can be found in the following
Instructions for Use chapters:
The anterior-posterior position is also an effective
placement (Figure 9).
Figure 9
Anterior-Posterior Position
•
HeartStart MRx M3535A/M3536A Chapter 17:
Configuration
•
HeartStart XL+ Chapter 13: Configuration
Note that the HeartStart XL default pacer settings are not
configurable.
Changing Rate and Output (mA) During an
Event
The pacer rate can be adjusted during pacing from the
default configuration by pressing the [Pacer Rate] soft
key on the device and then the navigational keys to select
the desired number of pace pulses per minute. The pacer
output can also be adjusted during pacing from the
default configuration by pressing the [Pacer Output] soft
key and then the navigational keys to:
Monitoring Electrodes
When performing demand mode pacing, the patient
must be monitored through either 3- or 5-lead
monitoring electrodes. Philips’ ALS defibrillator/
monitors use the heart rate from this monitoring source
to determine if a paced pulse should be delivered.
Monitoring electrodes are not required for fixed mode
pacing.
Setting Pacing Rate and Pacing
Output (mA)
Setting the Default Configuration
The HeartStart MRx and HeartStart XL+ allow you to
customize the defibrillator to best meet your needs with
configurable default pacer rate and output settings.
Configuration is performed through Configuration
mode of the device and may be saved to a data card for
replication on multiple devices. At any time,
configuration settings may be viewed and exported to a
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a. Increase the output until electrical capture occurs.
Electrical capture is indicated by the appearance of a
QRS complex after each pacing marker.
b. Decrease the output to the lowest level that still
maintains capture.
Presence of a peripheral pulse must be verified to assess
mechanical capture.
Further reference can be found in the following
Instructions for Use chapters:
•
HeartStart MRx M3535A/M3536A Chapter 7:
Noninvasive Pacing
•
HeartStart XL+ Chapter 8: Pacing
•
HeartStart XL Chapter 8: Pacing
During pacing, verify that white markers (on the MRx)
or arrows (on the XL+) appear above the R-wave on the
ECG waveform. A single marker or arrow should be
associated with each R-wave. If the markers or arrows do
not appear or do not coincide with the R-wave, select
another lead. Press the Lead Select button to select the
best lead with an easily detectable R-wave. If you are
using anterior-anterior pads placement while pacing and
are experiencing difficulty with Lead II, select another
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Non-Invasive Transcutaneous Pacing
lead. If a lead cannot be found with correct markers or
arrows above the R-waves, then switch to fixed mode
pacing.
Changing to Fixed Mode Pacing During an
Event
With the HeartStart MRx and HeartStart XL+, you can
switch to fixed mode pacing during an event, as follows:
A pulse oximeter is a powerful tool when used in
conjunction with the pacer/ECG monitor for confirming
capture because both mechanical and electrical activities
can be measured. ECRI provided a theoretical and an
operational overview of non-invasive pacemakers and
concluded that monitoring ECG alone is not enough to
verify that the patient’s heart is providing cardiac output.
The article states that:
Press the [Pause Pacing] soft key and acknowledge the
message prompt.
Clear recognition of capture continues to be a
2.
Press the Menu Select button and select Pacer Mode.
Artifact from skeletal muscle contractions induced by
3.
Use the Navigational buttons to highlight Fixed and
press the Menu Select button.
4.
Press the [Resume Pacing] soft key to resume pacing in
fixed mode.
pacing stimuli can mimic a captured waveform,
making verification of capture with the ECG alone
unreliable.
1.
With the HeartStart XL, the user can switch to fixed
mode pacing by pressing the Mode key.
Further reference can be found in the following
Instructions for Use chapters:
•
HeartStart MRx M3535A/M3536A Chapter 7:
Noninvasive Pacing
•
HeartStart XL+ Chapter 8: Pacing
•
HeartStart XL Chapter 8: Pacing
What to Look for When Pacing
Cardiac Capture
Capture is defined as gaining control of the patient’s
dysfunctional heart by an electrical stimulus (that is,
depolarization). Electrical capture can be determined by
observing the monitor, which should show a clear
indication of the ECG and the pulse marker. Skeletal
muscle contraction is not an indication that capture has
been established, nor is electrical capture alone an
indication of effective cardiac perfusion. The patient may
be suffering from pulseless electrical activity (PEA),
previously referred to as electromechanical dissociation
(EMD). When the patient is successfully paced:
challenge with today’s non-invasive pacemakers.
Electrical capture does not always produce an effective
mechanical (cardiac) contraction.
Therefore, a patient’s response to pacing must be verified
by signs of improved cardiac output, such as: a palpable
pulse rate the same as the rate which pace pulses are being
delivered, a rise in blood pressure, and/or improved skin
color.
An integral or standalone pulse oximeter can be useful for
confirming capture (by comparing the pulse rate
measured by the pulse oximeter to the set pacing rate)
and perfusion (by measuring blood oxygen saturation,
SpO2)11. Philips’ defibrillator/monitors integrate the
optional SpO2 package into the defibrillator for speed,
simplicity, and convenience. The SpO2 percentage (%)
and SpO2 alarm violations will be recorded in the Event
Summary.
Another important factor in effective pacing is the
amount of current applied. Sufficient current must be
applied to stimulate the heart into contractions. Unlike
invasive pacemakers, non-invasive pacemakers must pass
electrical current through the skin and thorax. This
requires significantly higher current. The higher current
loads can cause the chest muscles to contract and relax
strenuously, which may be painful and distressing for the
patient.
cardiac output may improve
Using the lowest output setting necessary to achieve
capture will minimize the discomfort. If the discomfort is
intolerable, sedation and/or analgesia may be necessary.
the patient’s pulse rate is at least equal to the pacer
Patient Discomfort
electrical and mechanical capture are achieved
rate
Pacing will likely cause some discomfort in conscious
patients. Two types of discomfort often experienced are a
burning sensation at the electrode site, and muscle
contraction. Thus, setting the expectations with the
blood pressure may improve
skin color may improve
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Special Pacing Situations
patient and family is very important. This should
alleviate any anxiety or tension and allow the patient to
become more relaxed. Patients should always be
comforted throughout the procedure, and sedation may
be necessary. Make sure the pads are positioned according
to the manufacturer’s recommendation. Avoid placing
the pads directly over lesions, injuries or large bone
structures (sternum, spine, scapula). Otherwise, more
pacer output will be needed to achieve capture.
Special Pacing Situations
Pediatric Pacing
Pain Threshold
If transcutaneous pacing is elected, the physiological
differences between adults and pediatric patients must be
considered:
The discomfort associated with pacing may necessitate
sedation in younger conscious children.
Electrode Size per AAMI Specification
The use of Lead II is not recommended when using
anterior-anterior lead placement.
adult — total active area of both pads combined
should be at least 150 cm2. Adult pads are
recommended for use on children weighing 10 kg or
more.
pediatric — total active area of both pads combined
should be at least 45 cm2. Recommended for use on
children weighing less than 10kg.
See ANSI/AAMI DF2-1996.
Skin Fragility
Electrodes should be checked frequently (every thirty
minutes) to avoid burns and should not be left on for
more than two hours.
Lead Placement
NOTE: Unlike adult pacing, the use of pediatric
transcutaneous pacing will likely be limited for
cardiopulmonary arrest since most complications are
precipitated by respiratory failure rather than by a
primary cardiac problem14.
Defibrillation During Pacing
In defibrillator/pacer combinations, Philips defibrillators
will automatically terminate pacing once the defibrillator
charge switch is enabled.
Higher Heart Rate
100 BPM is considered tachycardia in adults. A heart
rate less than 100 BPM is considered bradycardia in a
neonate.
Supraventricular tachycardia is faster in children than
in adults (the heart rate is typically 300 BPM in
infants younger than three months of age).
Supraventricular tachycardia is more common than
ventricular tachycardia in children.
Atrial flutter is faster in children than in adults.
Newborns may have rates of 600 BPM with distinct
P-waves. The usual ventricular rate in a newborn with
atrial flutter is 200 to 300 BPM12.
Ventricular tachycardia in infants under the age of
two years averages 260 BPM, which is similar to the
rates for supraventricular tachycardia13.
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Non-Invasive Transcutaneous Pacing
Troubleshooting Transcutaneous Pacing
1.
Check electrode/patient contact.
Check electrode connections.
ECG signal may be too noisy (see below).
Is there discomfort or pain during pacing?
Explain and set expectations with the patient on
the procedure. Comfort and provide
encouragement to the patient.
Make sure electrodes have been applied following
5.
Was the patient’s skin clean and dry and excessive
manufacturer’s guidelines. Electrodes should not
be placed over bone (i.e. on the sternum or
scapula).
hair removed prior to electrode attachment?
Was the expiration date checked before applying
the electrodes? Dry gel will have an adverse effect
on the ECG signal.
Consider analgesia or sedation.
2.
Is there electrical capture?
Check the electrode connections.
Were the electrodes positioned according to the
Pacer output may be too low. Increase pacer
output.
Observe the ECG monitor and not just the
patient. Electrical capture occurs when there is a
consistent ST segment and T-wave after each
spike.
Check electrode placement.
Check contact between the electrode and the
patient.
Check to see if the pacer is turned on.
Check viability of the patient.
3.
Is there mechanical capture?
Check pulse (palpate).
Check pulse oximeter (SpO2).
Check blood pressure.
Check skin color.
Evaluate mental status of patient.
4.
Is the pacer not sensing heart rate in demand mode?
Check size of R-wave. If it is too small, increase
the ECG size.
Check to see if the pacer is turned on.
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Is there a noisy ECG signal?
manufacturer’s guidelines?
6.
Is there redness or burns after electrode removal?
Ring-shaped erythema can be expected after
pacing. The appearance is similar to the erythema
seen after receiving shocks from standard external
paddle sets. The reaction may vary from patient to
patient due to a number of variables: skin
composition, medication at the time of pacing,
age (very young and older patients may be more
prone to erythema), dehydration, length of time
the patient was paced, and improper pads
application. Case reports of burns on neonates and
children have been documented. In most cases,
the children had numerous other complications
which may have contributed to the burns.
Neonates in particular may be more susceptible to
thermal injury than adults due to thinner skin, less
hair, weaker intercellular attachments, fewer
eccrine and sebaceous gland secretions, and an
increased susceptibility to external irritants. To
minimize thermal injury, pacing duration should
be kept to a minimum with frequent skin
inspection (every 30 minutes)15.
References
References
1
2
3
4
5
6
Rudd M. Basic concepts of cardiovascular physiology. Hewlett
Packard Company, 1973, Mar; 7:1-8:4.
American Heart Association, ACLS Provider Manual, 2002
Zoll P.M., “Non-invasive temporary cardiac pacing.”
Journal of Electrophysiology, 1987; 1:156-161.
Luck J.C., Davis D. “Termination of sustained tachycardia
by external non-invasive pacing.” PACE, 1987;
10:1125-1270.
Barold S.S., Falkoff M.D., Ong L.S., et al. “Termination of
ventricular tachycardia by transcutaneous cardiac pacing.”
American Heart Journal, 1987; 114:180-182.
Bartecchi C.E. “Temporary cardiac pacing — Diagnostic
and therapeutic indications.” Postgraduate Medicine, 1987
June; 81(8):269-77.
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8
9
10
11
ECRI. Reprinted with permission from Health Devices,
1993:22(3-4):216.
Garson A. “Pediatric arrhythmias. How different from
adults?” Med. Surg. Ped., 1987; 9: 543-52.
Garson A., Smith R.T., Cooley D.A., et al. “Incessant
ventricular tachycardia in infants: Purkinje hamartomas
and surgical cure”. J Am Col Card, publication pending.
Beland M.J., Hesslein P.S., Finlay C.D., et al.
“Non-invasive transcutaneous cardiac pacing in children”.
PACE, 1987 Nov-Dec; 10:1262-70.
Pride H.B., McKinley D.F. “Third degree burns from the
use of an external cardiac pacing device.” Critical Care
Medicine, 1990; 18(5):572-73.
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Non-Invasive Transcutaneous Pacing
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Koninklijke Philips Electronics N.V.
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Published Feb. 2013, Edition 2
Printed in the USA
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